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active recombinant aurka protein  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc active recombinant aurka protein
    (A) Effect of gossypin on EGF-induced activation of various signaling proteins in JB6 cells. Serum-starved (0.1% FBS; 48 h) JB6 cells were treated with various doses of gossypin for 2 h followed by treatment with EGF for 30 min. (B) Effect of gossypin on various signaling proteins in HGC27 gastric cancer cells. Cells were treated with gossypin and then signaling pathway proteins were detected by Western blotting. (C) Gossypin inhibits phosphorylation of histone H3 in AGS gastric cancer cells. Cells were treated with gossypin for 24 h and detected by immunofluorescence assay. Red color indicates phosphorylated histone H3 at serine 10 and blue color shows DAPI. (D-E) Gossypin suppresses <t>AURKA</t> and RSK2 kinase activity in a dose-dependent manner. The effect of gossypin on AURKA or RSK2 activity was assessed by an in vitro kinase assay using AURKA (active, 200 ng) and MBP (AURKA substrate, 400 ng) or RSK2 (active, 200 ng) and ATF1 (RSK2 substrate, 300 ng) proteins. The effect of gossypin on kinase activities was determined by Western blotting using an antibody to detect phosphorylated serine and threonine. Band density was measured using the Image J (NIH) software program. For all data, similar results were obtained from 3 independent experiments.
    Active Recombinant Aurka Protein, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Gossypin inhibits gastric cancer growth by direct targeting AURKA and RSK2"

    Article Title: Gossypin inhibits gastric cancer growth by direct targeting AURKA and RSK2

    Journal: Phytotherapy research : PTR

    doi: 10.1002/ptr.6253

    (A) Effect of gossypin on EGF-induced activation of various signaling proteins in JB6 cells. Serum-starved (0.1% FBS; 48 h) JB6 cells were treated with various doses of gossypin for 2 h followed by treatment with EGF for 30 min. (B) Effect of gossypin on various signaling proteins in HGC27 gastric cancer cells. Cells were treated with gossypin and then signaling pathway proteins were detected by Western blotting. (C) Gossypin inhibits phosphorylation of histone H3 in AGS gastric cancer cells. Cells were treated with gossypin for 24 h and detected by immunofluorescence assay. Red color indicates phosphorylated histone H3 at serine 10 and blue color shows DAPI. (D-E) Gossypin suppresses AURKA and RSK2 kinase activity in a dose-dependent manner. The effect of gossypin on AURKA or RSK2 activity was assessed by an in vitro kinase assay using AURKA (active, 200 ng) and MBP (AURKA substrate, 400 ng) or RSK2 (active, 200 ng) and ATF1 (RSK2 substrate, 300 ng) proteins. The effect of gossypin on kinase activities was determined by Western blotting using an antibody to detect phosphorylated serine and threonine. Band density was measured using the Image J (NIH) software program. For all data, similar results were obtained from 3 independent experiments.
    Figure Legend Snippet: (A) Effect of gossypin on EGF-induced activation of various signaling proteins in JB6 cells. Serum-starved (0.1% FBS; 48 h) JB6 cells were treated with various doses of gossypin for 2 h followed by treatment with EGF for 30 min. (B) Effect of gossypin on various signaling proteins in HGC27 gastric cancer cells. Cells were treated with gossypin and then signaling pathway proteins were detected by Western blotting. (C) Gossypin inhibits phosphorylation of histone H3 in AGS gastric cancer cells. Cells were treated with gossypin for 24 h and detected by immunofluorescence assay. Red color indicates phosphorylated histone H3 at serine 10 and blue color shows DAPI. (D-E) Gossypin suppresses AURKA and RSK2 kinase activity in a dose-dependent manner. The effect of gossypin on AURKA or RSK2 activity was assessed by an in vitro kinase assay using AURKA (active, 200 ng) and MBP (AURKA substrate, 400 ng) or RSK2 (active, 200 ng) and ATF1 (RSK2 substrate, 300 ng) proteins. The effect of gossypin on kinase activities was determined by Western blotting using an antibody to detect phosphorylated serine and threonine. Band density was measured using the Image J (NIH) software program. For all data, similar results were obtained from 3 independent experiments.

    Techniques Used: Activation Assay, Western Blot, Phospho-proteomics, Immunofluorescence, Activity Assay, In Vitro, Kinase Assay, Software

    (A) Modeling of gossypin binding with AURKA at the ATP binding pocket (left panel); and Ligand Interaction Diagram (LID) of the binding (upper right panel). (B) Modeling of gossypin binding with the N-terminal domain (NTD) at the ATP binding pocket of RSK2 (upper left panel) and LID of the binding (upper right panel). Modeling of gossypin binding with the C-terminal domain (CTD) at the ATP binding pocket of RSK2 (lower left panel) and LID of the binding (lower right panel). The AURKA, NTD RSK2 and CTD RSK2 structures are shown as ribbon representation and gossypin is shown as stick representation. LID legend is shown below. Gossypin directly binds to AURKA or RSK2 in (C) gastric cancer cell lysates or (D) as recombinant proteins. The recombinant proteins or cell lysates were incubated with gossypin-conjugated Sepharose 4B beads or with Sepharose 4B beads alone. The pulled down proteins were analyzed by Western blotting. For C and D, similar results were obtained from 3 independent experiments.
    Figure Legend Snippet: (A) Modeling of gossypin binding with AURKA at the ATP binding pocket (left panel); and Ligand Interaction Diagram (LID) of the binding (upper right panel). (B) Modeling of gossypin binding with the N-terminal domain (NTD) at the ATP binding pocket of RSK2 (upper left panel) and LID of the binding (upper right panel). Modeling of gossypin binding with the C-terminal domain (CTD) at the ATP binding pocket of RSK2 (lower left panel) and LID of the binding (lower right panel). The AURKA, NTD RSK2 and CTD RSK2 structures are shown as ribbon representation and gossypin is shown as stick representation. LID legend is shown below. Gossypin directly binds to AURKA or RSK2 in (C) gastric cancer cell lysates or (D) as recombinant proteins. The recombinant proteins or cell lysates were incubated with gossypin-conjugated Sepharose 4B beads or with Sepharose 4B beads alone. The pulled down proteins were analyzed by Western blotting. For C and D, similar results were obtained from 3 independent experiments.

    Techniques Used: Binding Assay, Recombinant, Incubation, Western Blot



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    Image Search Results


    The correlation analysis between hub genes and OS of patients with ovarian cancer. The association between the expression levels of AURKA ( A ), BUB1 ( B ), BUB1B ( C ), CENPF ( D ), KIF11 ( E ), KIF23 ( F ) and TOP2A ( G ) and the OS of patients with ovarian cancer was analyzed by KM plotter ( www.kmplot.com ).

    Journal: Cancer Management and Research

    Article Title: Identification of the Hub Genes Associated with the Prognosis of Ovarian Cancer Patients via Integrated Bioinformatics Analysis and Experimental Validation

    doi: 10.2147/CMAR.S282529

    Figure Lengend Snippet: The correlation analysis between hub genes and OS of patients with ovarian cancer. The association between the expression levels of AURKA ( A ), BUB1 ( B ), BUB1B ( C ), CENPF ( D ), KIF11 ( E ), KIF23 ( F ) and TOP2A ( G ) and the OS of patients with ovarian cancer was analyzed by KM plotter ( www.kmplot.com ).

    Article Snippet: The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Techniques: Expressing

    The correlation analysis between hub genes and PFS of patients with ovarian cancer. The association between the expression levels of AURKA ( A ), BUB1B ( B ), CENPF ( C ), KIF11 ( D ), KIF23 ( E ) and TOP2A ( F ) and the PFS of patients with ovarian cancer was analyzed by KM plotter ( www.kmplot.com ).

    Journal: Cancer Management and Research

    Article Title: Identification of the Hub Genes Associated with the Prognosis of Ovarian Cancer Patients via Integrated Bioinformatics Analysis and Experimental Validation

    doi: 10.2147/CMAR.S282529

    Figure Lengend Snippet: The correlation analysis between hub genes and PFS of patients with ovarian cancer. The association between the expression levels of AURKA ( A ), BUB1B ( B ), CENPF ( C ), KIF11 ( D ), KIF23 ( E ) and TOP2A ( F ) and the PFS of patients with ovarian cancer was analyzed by KM plotter ( www.kmplot.com ).

    Article Snippet: The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Techniques: Expressing

    Expression analysis of hub genes. The expression levels of AURKA ( A ), BUB1B ( B ), CENPF ( C ), KIF11 ( D ), KIF23 ( E ) and TOP2A ( F ) in ovarian cancer tissues and normal ovarian tissues were analyzed by GEPIA tool. * P < 0.05.

    Journal: Cancer Management and Research

    Article Title: Identification of the Hub Genes Associated with the Prognosis of Ovarian Cancer Patients via Integrated Bioinformatics Analysis and Experimental Validation

    doi: 10.2147/CMAR.S282529

    Figure Lengend Snippet: Expression analysis of hub genes. The expression levels of AURKA ( A ), BUB1B ( B ), CENPF ( C ), KIF11 ( D ), KIF23 ( E ) and TOP2A ( F ) in ovarian cancer tissues and normal ovarian tissues were analyzed by GEPIA tool. * P < 0.05.

    Article Snippet: The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Techniques: Expressing

    Protein expression of hub genes. The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Journal: Cancer Management and Research

    Article Title: Identification of the Hub Genes Associated with the Prognosis of Ovarian Cancer Patients via Integrated Bioinformatics Analysis and Experimental Validation

    doi: 10.2147/CMAR.S282529

    Figure Lengend Snippet: Protein expression of hub genes. The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Article Snippet: The protein expression of AURKA ( A ), CENPF ( B ), KIF11 ( C ), KIF23 ( D ) and TOP2A ( E ) in ovarian cancer tissues and normal ovarian tissues were extracted from the Human Protein Atlas ( http://www.proteinatlas.org/ ).

    Techniques: Expressing

    (A) Effect of gossypin on EGF-induced activation of various signaling proteins in JB6 cells. Serum-starved (0.1% FBS; 48 h) JB6 cells were treated with various doses of gossypin for 2 h followed by treatment with EGF for 30 min. (B) Effect of gossypin on various signaling proteins in HGC27 gastric cancer cells. Cells were treated with gossypin and then signaling pathway proteins were detected by Western blotting. (C) Gossypin inhibits phosphorylation of histone H3 in AGS gastric cancer cells. Cells were treated with gossypin for 24 h and detected by immunofluorescence assay. Red color indicates phosphorylated histone H3 at serine 10 and blue color shows DAPI. (D-E) Gossypin suppresses AURKA and RSK2 kinase activity in a dose-dependent manner. The effect of gossypin on AURKA or RSK2 activity was assessed by an in vitro kinase assay using AURKA (active, 200 ng) and MBP (AURKA substrate, 400 ng) or RSK2 (active, 200 ng) and ATF1 (RSK2 substrate, 300 ng) proteins. The effect of gossypin on kinase activities was determined by Western blotting using an antibody to detect phosphorylated serine and threonine. Band density was measured using the Image J (NIH) software program. For all data, similar results were obtained from 3 independent experiments.

    Journal: Phytotherapy research : PTR

    Article Title: Gossypin inhibits gastric cancer growth by direct targeting AURKA and RSK2

    doi: 10.1002/ptr.6253

    Figure Lengend Snippet: (A) Effect of gossypin on EGF-induced activation of various signaling proteins in JB6 cells. Serum-starved (0.1% FBS; 48 h) JB6 cells were treated with various doses of gossypin for 2 h followed by treatment with EGF for 30 min. (B) Effect of gossypin on various signaling proteins in HGC27 gastric cancer cells. Cells were treated with gossypin and then signaling pathway proteins were detected by Western blotting. (C) Gossypin inhibits phosphorylation of histone H3 in AGS gastric cancer cells. Cells were treated with gossypin for 24 h and detected by immunofluorescence assay. Red color indicates phosphorylated histone H3 at serine 10 and blue color shows DAPI. (D-E) Gossypin suppresses AURKA and RSK2 kinase activity in a dose-dependent manner. The effect of gossypin on AURKA or RSK2 activity was assessed by an in vitro kinase assay using AURKA (active, 200 ng) and MBP (AURKA substrate, 400 ng) or RSK2 (active, 200 ng) and ATF1 (RSK2 substrate, 300 ng) proteins. The effect of gossypin on kinase activities was determined by Western blotting using an antibody to detect phosphorylated serine and threonine. Band density was measured using the Image J (NIH) software program. For all data, similar results were obtained from 3 independent experiments.

    Article Snippet: The active recombinant AURKA (300 ng) or RSK2 (200 ng) protein was mixed with different concentrations of gossypin in reaction buffer (Cell Signaling Technology) and incubated at room temperature for 15 min.

    Techniques: Activation Assay, Western Blot, Phospho-proteomics, Immunofluorescence, Activity Assay, In Vitro, Kinase Assay, Software

    (A) Modeling of gossypin binding with AURKA at the ATP binding pocket (left panel); and Ligand Interaction Diagram (LID) of the binding (upper right panel). (B) Modeling of gossypin binding with the N-terminal domain (NTD) at the ATP binding pocket of RSK2 (upper left panel) and LID of the binding (upper right panel). Modeling of gossypin binding with the C-terminal domain (CTD) at the ATP binding pocket of RSK2 (lower left panel) and LID of the binding (lower right panel). The AURKA, NTD RSK2 and CTD RSK2 structures are shown as ribbon representation and gossypin is shown as stick representation. LID legend is shown below. Gossypin directly binds to AURKA or RSK2 in (C) gastric cancer cell lysates or (D) as recombinant proteins. The recombinant proteins or cell lysates were incubated with gossypin-conjugated Sepharose 4B beads or with Sepharose 4B beads alone. The pulled down proteins were analyzed by Western blotting. For C and D, similar results were obtained from 3 independent experiments.

    Journal: Phytotherapy research : PTR

    Article Title: Gossypin inhibits gastric cancer growth by direct targeting AURKA and RSK2

    doi: 10.1002/ptr.6253

    Figure Lengend Snippet: (A) Modeling of gossypin binding with AURKA at the ATP binding pocket (left panel); and Ligand Interaction Diagram (LID) of the binding (upper right panel). (B) Modeling of gossypin binding with the N-terminal domain (NTD) at the ATP binding pocket of RSK2 (upper left panel) and LID of the binding (upper right panel). Modeling of gossypin binding with the C-terminal domain (CTD) at the ATP binding pocket of RSK2 (lower left panel) and LID of the binding (lower right panel). The AURKA, NTD RSK2 and CTD RSK2 structures are shown as ribbon representation and gossypin is shown as stick representation. LID legend is shown below. Gossypin directly binds to AURKA or RSK2 in (C) gastric cancer cell lysates or (D) as recombinant proteins. The recombinant proteins or cell lysates were incubated with gossypin-conjugated Sepharose 4B beads or with Sepharose 4B beads alone. The pulled down proteins were analyzed by Western blotting. For C and D, similar results were obtained from 3 independent experiments.

    Article Snippet: The active recombinant AURKA (300 ng) or RSK2 (200 ng) protein was mixed with different concentrations of gossypin in reaction buffer (Cell Signaling Technology) and incubated at room temperature for 15 min.

    Techniques: Binding Assay, Recombinant, Incubation, Western Blot

    AURKA was upregulated in colon cancer and predicted a benefit outcome. (a) Compared with the matched normal tissues, AURKA was significantly upregulated in cancer tissues in 15 out of 18 cancer types. (b) AURKA expression level was adversely correlated with OS in 5 of 15 cancers but positively correlated with OS in COAD.

    Journal: BioMed Research International

    Article Title: AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes

    doi: 10.1155/2020/8916729

    Figure Lengend Snippet: AURKA was upregulated in colon cancer and predicted a benefit outcome. (a) Compared with the matched normal tissues, AURKA was significantly upregulated in cancer tissues in 15 out of 18 cancer types. (b) AURKA expression level was adversely correlated with OS in 5 of 15 cancers but positively correlated with OS in COAD.

    Article Snippet: The membrane was incubated with primary antibodies: AURKA rabbit polyclonal antibody (ProteinTech, Wuhan, China.

    Techniques: Expressing

    Undermethylation, upregulation of TFs, and gene amplification potentially contributed to the elevated expression of AURKA. (a) Five methylation sites in AURKA DNA were significantly adversely correlated with the level of AURKA. (b) Based on the public data analysis, a total of 159 TFs potentially regulated AURKA transcription. The expression of 85 TFs was positively correlated with the level of AURKA. Moreover, 15 of them have been identified to be overexpressed in colon cancer tissues compared with the matched normal tissues. (c, d) The expression of the top four TFs highly correlated with AURKA was higher in colon cancer tissues compared with normal tissues. (e) The expression level of AURKA in the AURKA CNV gain group was significantly higher than that in the AURKA CNV neutral group in COAD.

    Journal: BioMed Research International

    Article Title: AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes

    doi: 10.1155/2020/8916729

    Figure Lengend Snippet: Undermethylation, upregulation of TFs, and gene amplification potentially contributed to the elevated expression of AURKA. (a) Five methylation sites in AURKA DNA were significantly adversely correlated with the level of AURKA. (b) Based on the public data analysis, a total of 159 TFs potentially regulated AURKA transcription. The expression of 85 TFs was positively correlated with the level of AURKA. Moreover, 15 of them have been identified to be overexpressed in colon cancer tissues compared with the matched normal tissues. (c, d) The expression of the top four TFs highly correlated with AURKA was higher in colon cancer tissues compared with normal tissues. (e) The expression level of AURKA in the AURKA CNV gain group was significantly higher than that in the AURKA CNV neutral group in COAD.

    Article Snippet: The membrane was incubated with primary antibodies: AURKA rabbit polyclonal antibody (ProteinTech, Wuhan, China.

    Techniques: Amplification, Expressing, Methylation

    AURKA increased the chemosensitivity of colon cancer cells to Oxaliplatin. (a) AURKA was upregulated or knocked down in two cancer cell lines. (b, c) AURKA overexpression promoted the death of HCT116 and SW1116 colon cancer cells induced by Oxaliplatin, whereas knockdown of AURKA significantly weakened the response of colon cancer cells to Oxaliplatin.

    Journal: BioMed Research International

    Article Title: AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes

    doi: 10.1155/2020/8916729

    Figure Lengend Snippet: AURKA increased the chemosensitivity of colon cancer cells to Oxaliplatin. (a) AURKA was upregulated or knocked down in two cancer cell lines. (b, c) AURKA overexpression promoted the death of HCT116 and SW1116 colon cancer cells induced by Oxaliplatin, whereas knockdown of AURKA significantly weakened the response of colon cancer cells to Oxaliplatin.

    Article Snippet: The membrane was incubated with primary antibodies: AURKA rabbit polyclonal antibody (ProteinTech, Wuhan, China.

    Techniques: Over Expression, Knockdown

    AURKA downregulated the expression of DDR genes by inhibiting TP53. (a, b) Overexpression of AURKA promoted the phosphorylation of TP53 and decreased the level of total TP53, whereas knockdown of AURKA reduced the phosphorylation of TP53 and increased the level of total TP53 in colon cancer cells by immunoblot. AURKA had no effect on the expression of MDM2. (c, d) Six representative DDR genes were downregulated in colon cancer cells with AURKA overexpression but upregulated when knocking down AURKA in colon cancer cells by real-time PCR.

    Journal: BioMed Research International

    Article Title: AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes

    doi: 10.1155/2020/8916729

    Figure Lengend Snippet: AURKA downregulated the expression of DDR genes by inhibiting TP53. (a, b) Overexpression of AURKA promoted the phosphorylation of TP53 and decreased the level of total TP53, whereas knockdown of AURKA reduced the phosphorylation of TP53 and increased the level of total TP53 in colon cancer cells by immunoblot. AURKA had no effect on the expression of MDM2. (c, d) Six representative DDR genes were downregulated in colon cancer cells with AURKA overexpression but upregulated when knocking down AURKA in colon cancer cells by real-time PCR.

    Article Snippet: The membrane was incubated with primary antibodies: AURKA rabbit polyclonal antibody (ProteinTech, Wuhan, China.

    Techniques: Expressing, Over Expression, Phospho-proteomics, Knockdown, Western Blot, Real-time Polymerase Chain Reaction